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目录产品 » 稳定细胞系 » Human Recombinant Adenosine A3 Receptor Stable Cell Line
CHO-K1/ADORA3/Gα15 Stable Cell Line

Figure 1. NECA-induced concentration-dependent stimulation of intracellular calcium mobilization in CHO-K1/ADORA3/Gα15 cells. The cells were loaded with Calcium-4 prior to being stimulated with an ADORA3 receptor agonist, NECA. The intracellular calcium change was measured by FLIPR. The relative fluorescence unit (RFU) were normalized and plotted against the log of the cumulative doses of NECA (Mean ± SEM, n = 3). The EC50 of NECA on this cell was 4.76 nM.
Notes:
1. EC50 value is calculated with four parameter logistic equation:
Y=Bottom + (Top-Bottom)/(1+10^((LogEC50-X)*HillSlope))
X is the logarithm of concentration. Y is the response
Y is RFU and starts at Bottom and goes to Top with a sigmoid shape.
2. Signal to background Ratio (S/B) = Top/Bottom

CHO-K1/ADORA3/Gα15 Stable Cell Line

Extracellular adenosine mediates a multitude of biological effects, including wakefulness, antiarrythmia, bronchoconstriction and response to ischemia and oxidative stress. A family of four G-protein coupled adrenoceptors, A1, A2A, A2B and A3, is responsible for these effects. A3, which couples to Gi/o, is expressed in a wide range of human tissues, but most predominantly in the lung and liver. Recent animal model studies have shown that A3 receptors play important roles in brain ischemia, immunosuppresion, and bronchospasm. A3 receptor agonists and/or agonists may have important clinical value in the treatment of asthma and inflammation. Mice lacking A3 receptors display reduced mast cell degranulation and bronchoconstriction in response to adenosine.
M00464
￥85000

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Description

Extracellular adenosine mediates a multitude of biological effects, including wakefulness, antiarrythmia, bronchoconstriction and response to ischemia and oxidative stress. A family of four G-protein coupled adrenoceptors, A1, A2A, A2B and A3, is responsible for these effects. A3, which couples to Gi/o, is expressed in a wide range of human tissues, but most predominantly in the lung and liver. Recent animal model studies have shown that A3 receptors play important roles in brain ischemia, immunosuppresion, and bronchospasm. A3 receptor agonists and/or agonists may have important clinical value in the treatment of asthma and inflammation. Mice lacking A3 receptors display reduced mast cell degranulation and bronchoconstriction in response to adenosine.
Synonyms

A3 receptor, adenosine A3 receptor, TGPCR1, ARA3, A3AR, A3R, AA3R

Applications Functional assays for ADORA3 receptor

Storage Liquid nitrogen immediately upon delivery
Species Human

Freeze Medium 45% culture medium, 45% FBS (Cat. #10099-141, Gibco), 10% DMSO (Cat. #D2650, Sigma)
Culture Medium Ham’s F-12K (Kaighn’s), 10% FBS, 100 μg/ml Hygromycin B (Cat. #10687010, Invitrogen), 8 ug/ml Puromycin (Cat. #A11138-03, Gibco)

  • CHO-K1/ADORA3/Gα15 Stable Cell Line
    • CHO-K1/ADORA3/Gα15 Stable Cell Line

    Figure 1. NECA-induced concentration-dependent stimulation of intracellular calcium mobilization in CHO-K1/ADORA3/Gα15 cells. The cells were loaded with Calcium-4 prior to being stimulated with an ADORA3 receptor agonist, NECA. The intracellular calcium change was measured by FLIPR. The relative fluorescence unit (RFU) were normalized and plotted against the log of the cumulative doses of NECA (Mean ± SEM, n = 3). The EC50 of NECA on this cell was 4.76 nM.
    Notes:
    1. EC50 value is calculated with four parameter logistic equation:
    Y=Bottom + (Top-Bottom)/(1+10^((LogEC50-X)*HillSlope))
    X is the logarithm of concentration. Y is the response
    Y is RFU and starts at Bottom and goes to Top with a sigmoid shape.
    2. Signal to background Ratio (S/B) = Top/Bottom


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